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Interactions between the host and its microbiota are of mutual benefit and promote health. Complex molecular pathways underlie this dialog, but the identity of microbe-derived molecules that mediate the mutualistic state remains elusive. Helicobacter hepaticus is a member of the mouse intestinal microbiota that is tolerated by the host. In the absence of an intact IL-10 signaling, H. hepaticus induces an IL-23-driven inflammatory response in the intestine. Here we investigate the interactions between H. hepaticus and host immune cells that may promote mutualism, and the microbe-derived molecule(s) involved. Our results show that H. hepaticus triggers early IL-10 induction in intestinal macrophages and produces a large soluble polysaccharide that activates a specific MSK/CREB-dependent anti-inflammatory and repair gene signature via the receptor TLR2. These data identify a host-bacterial interaction that promotes mutualistic mechanisms at the intestinal interface. Further understanding of this pathway may provide novel prevention and treatment strategies for inflammatory bowel disease.

Original publication

DOI

10.1016/j.chom.2017.11.002

Type

Journal article

Journal

Cell Host Microbe

Publication Date

13/12/2017

Volume

22

Pages

733 - 745.e5

Keywords

CREB, Helicobacter hepaticus, MSK1/2, TLR2, anti-inflammatory gene signature, host-microbe interactions, inflammatory bowel disease, macrophage, mutualism, polysaccharide, Animals, Helicobacter hepaticus, Immunosuppressive Agents, Interleukin-10, Interleukin-23, Macrophages, Mice, Polysaccharides, Bacterial, Symbiosis, Toll-Like Receptor 2